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Stromal cell‐derived factor‐1α improves infarcted heart function through angiogenesis in mice
Author(s) -
SASAKI TAKASHI,
FUKAZAWA RYUJI,
OGAWA SHUNICHI,
KANNO SHIGETO,
NITTA TAKASHI,
OCHI MASAMI,
SHIMIZU KAZUO
Publication year - 2007
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.2007.02491.x
Subject(s) - medicine , neovascularization , angiogenesis , myocardial infarction , infarction , arteriogenesis , ligation , bone marrow , cardiology , stromal cell , cardiac function curve , ischemia , stromal cell derived factor 1 , artery , heart failure , receptor , chemokine , cxcr4
Background: Local delivery of stromal cell‐derived factor‐1α (SDF‐1) has been demonstrated to improve hind limb ischemia through enhanced neovascularization in animals. It was hypothesized that local administration of SDF‐1 also contributes to neovascularization of ischemic heart. Method: Acute myocardial infarction was created by left coronary artery ligation in C57BL/6J mice. Immediately after infarction induction, mice were treated by injection directly into the center of ischemic myocardium either with saline (control group) or SDF‐1 (SDF‐1 group). Cardiac function was measured on echocardiogram 2 and 4 weeks after infarction. On week 4 mice were killed to evaluate infarction size and capillary vessel density. To determine the contribution of bone marrow cells to angiogenesis, the same procedures were performed on C57BL/6J chimeric mice reconstituted with green fluorescent protein‐positive bone marrow cells. Results: Fractional shortening was greater in the SDF‐1 group at 4 weeks (0.31 ± 0.06% vs 0.23 ± 0.03%, P = 0.037). The infarct area was smaller in the SDF‐1 group compared to the control group (9.31 ± 2.76% vs 18.07 ± 5.69%, P = 0.028). Green fluorescent protein‐positive cells accumulated predominantly at the peri‐infarction site, and were located with the capillary vessels. Capillary vessel density was significantly increased in the SDF‐1 group (13.08 ± 4.11 vessels/mm 2 vs 34.50 ± 7.59 vessels/mm 2 , P = 0.014). Conclusions: SDF‐1 protects against deterioration of cardiac function after acute myocardial infarction by promoting angiogenesis. The safety and long‐term prognosis of this treatment remains to be determined.